1. A case of psychiatric drug D.O. Clinical Toxicology Course Dr. Cynthia Shum UCH AED

2. History A 44-yr lady was brought in at 7:30pm by ambulance Suicidal attempt Took 20 tabs of drugs from 10am to 3pm and 10 tabs of another drug at 3pm

3. Vital signs: BP 101/70 Pulse 69/min Temp. 36.5 RR 20/min SpO2 100% on RA

4. Physical Examination GCS 15/15, pupils 3-4mm reactive Skin normal, bowel sound normal, no bladder Patient was upset, lethragic, tremor of hands was noted, but no weakness, no fasciculation, jerks not hyperactive

5. Bedside Investigation H ’ stix 3.5 ECG: SR normal QRS, QTc 0.46sec

6. PMH: Bipolar depression FU YFS On Lithium SR and clonazepam. Empty bags of Lithium SR (400mg/tab) and clonazepam (1mg/tab) found Total ingestion: Lithium SR 20tabs x 400mg = 8 gm Clonazepam 10tabs x 1mg = 10mg

7. What is your management? Investigations: Li level RFT Paracetamol/salicylate CBP INR AXR Decontamination Lavage AC Forced diuresis WBI: PEG 2L/hr until clear return

8. What ’ s your management? Supportive Fluid and electrolyte Adequate Hydration IVNS for good urine o/p Foley to BSB

9. Blood results: Li level 4.2mmol/L RFT normal Na, K normal CBP, INR normal Paracetamol/salicylate negative AXR: no tablets seen What else would you do?

10. Progress: ICU admission HD started 200-250ml/min x 3 hrs Patient was closely monitored and given bolus of fluid to maintain BP during HD

11. Acute Toxicity Action Level Chronic ToxicityWBI HD Time (Hour) From time of AED attendance

12. Lithium Sustained-Release Absorption: Delayed for 6-12 hrs, completed for another 8hrs Distribution Vd 0.6-0.9L/kg, Rapidly to blood, liver, kidney Metabolism Nil Elimination 95% by kidneys, minority by sweat & saliva T 1/2 20-24hrs

13. Clinical manifestation No/mild GI symptoms in SR form CNS: Mild:weakness, fine tremor, light headedness Moderate:muscle twitching, tinnitus, hyperreflexia, slurred speech, drowsiness, apathy Severe:confusion, clonus, choreoathetoid movement, seizure, coma

14. Acute on chronic toxicity CNS symptoms exclusively High total body burden of Li in chronic use Additional increase results in immediate toxicity Predisposing factors Continuation of high dose after acute mania Na restriction Intravascular volume depletion Decreased GFR Drug interation: NSAID, ACEI, SSRIs, antipsychotics

15. Laboratory testing RFT Look for the etiology of toxicity Predict response to conservative Rx Serial Li level Monitor response to therapy Reference Therapeutic level: 0.6-1.2 mmol/L Action level for acute toxicity: >4 mmol/L Action level for chronic toxicity: >1.5 mmol/L

16. Haemodialysis Who should get HD? When to initiate HD? Those who are initially poisoned and have high Li levels but no S/S of may benefit the most After Li has distributed the CNS, if is more difficult to remove by HD and permanent sequelae may occur

17. Who and when to HD? Symptoms Significant neurological symptoms Level Acute ingestion with Li >4mmol/L Acute on chronic with Li >1.5 mmol/L Failure of excretory pathway Renal failure Intolerable to Na repletion, e.g. CCF

18. Rebound Li level HD clears only the plasma Significant Li load in tissue Levels Immediate and 6hrs post HD Look for rebound

19. Thank you Q & A